We are investigating mechanisms by which prostaglandins produce changes in pulmonary function and circulaton. In addition, we are studying the interactions of changes in the lung in the pulmonary circulation produced by prostaglandins. In anesthetized, paralyzed, artificially ventilated dogs, we measure resistance of the respiratory system, dynamic compliance, pressures in the pulmonary artery and aorta, cardiac output, shunt fraction, and wasted ventilation, and serum concentrations of the products of arachidonic acid metabolism (e.g., PGF and E and their metabolites, prostacyclin and thromboxane) from the pulmonary artery and aorta. Morphologic studies include examination of the lungs and tantalum bronchography. In studies this year, we infused bradykinin intravenously (2 micrograms/kg/min.) into anesthetized, paralyzed, artificially ventilated mongrel dogs and measured lung pulmonary circulation function and measured transpulmonary (pulmonary artery and aorta) prostaglandin concentrations by radioimmunoassay. Respiratory system resistance, dynamic compliance, wasted ventilation and shunt fraction are not changed by bradykinin infusion. Furthermore, no evidence of arachidonic acid release nor prostaglandin F and E and prostaglandin E synthesis could be determined. In additional series of experiments, we produced hypoxia in our animal preparation during bradykinin infusions and determined transpulmonary prostaglandin concentrations and pulmonary circulation mechanics. Hypoxic stimulus failed to produce evidence of enhanced prostaglandin synthesis in these studies. Furthermore, no changes in pulmonary mechanics were noted. Pulmonary artery pressure increased 300% compared to control levels.